Actions of cytochalasins on the organization of actin filaments and microtubules in a neuronal growth cone.

Forscher, Paul; Smith, Stephen J.

doi:10.1083/jcb.107.4.1505

Cited by 813 publications

(682 citation statements)

References 47 publications

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“…Taken together, our observations are consistent with a model in which remodeling of the actin cytoskeleton in selected growth cones (e.g., those containing Tiam1) produces a loose actin meshwork in the central growth cone region that allows microtubule protrusion and thereafter process elongation (Forscher and Smith, 1988).…”

Section: Phosphorothioate Antisense Oligonucleotides Inhibit the Exprsupporting

confidence: 77%

“…Interestingly, cytochalasin D reverts the Tiam1 phenotype, with neurons extending one or more axons. It is likely that cytochalasin D replaces Tiam1 by allowing microtubules to penetrate any neuritic tip devoid of actin filaments and hence leads to multiple axon formation (Forscher and Smith, 1988;Bradke and Dotti, 1999). Interestingly, and as predicted by these results, overexpression of Tiam1 also results in the extension of several axon-like neurites, all of which are immunoreactive for Tiam1 and Tau1.…”

Section: Discussionsupporting

confidence: 49%

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Evidence for the Involvement of Tiam1 in Axon Formation

et al. 2001

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In cultured neurons, axon formation is preceded by the appearance in one of the multiple neurites of a large growth cone containing a labile actin network and abundant dynamic microtubules. The invasion-inducing T-lymphoma and metastasis 1 (Tiam1) protein that functions as a guanosine nucleotide exchange factor for Rac1 localizes to this neurite and its growth cone, where it associates with microtubules. Neurons overexpressing Tiam1 extend several axon-like neurites, whereas suppression of Tiam1 prevents axon formation, with most of the cells failing to undergo changes in growth cone size and in cytoskeletal organization typical of prospective axons. Cytochalasin D reverts this effect leading to multiple axon formation and penetration of microtubules within neuritic tips devoid of actin filaments. Taken together, these results suggest that by regulating growth cone actin organization and allowing microtubule invasion within selected growth cones, Tiam1 promotes axon formation and hence participates in neuronal polarization.

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Section: Phosphorothioate Antisense Oligonucleotides Inhibit the Exprsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 49%

Evidence for the Involvement of Tiam1 in Axon Formation

et al. 2001

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“…Actin monomers in the peripheral domain undergo constitutive plus end-directed filament assembly, elongating the filament in the distal tips of lamellipodia and filopodia and pushing the growth cone membrane in the forward direction; simultaneously the entire actin filament is dragged back by myosin-like molecular motors into the central domain where the actin filaments depolymerize (Forscher and Smith 1988;Tanaka and Sabry 1995;Mitchison and Cramer 1996). At the tail end of these actin filaments, the myosin-mediated retrograde flow blocks microtubules from advancing into the peripheral domain, and blocks the advance of the growth cone's central domain and therefore of the axon itself (Forscher and Smith 1988). The balance of anterograde polymerization and retrograde retraction determines the advance of these actin-rich structures in the peripheral domain; for example, blocking myosin activity causes filopodial elongation (Lin et al 1996).…”

Section: The Growth Cone: Motor and Clutch Of Axon Growthmentioning

confidence: 99%

How does an axon grow?

Goldberg¹

2003

Genes Dev.

204

138

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How do axons grow during development, and why do they fail to regrow when injured? In the complicated mesh of our nervous system, the axon is the information superhighway, carrying all of the data we use to sense our environment and carry out behaviors. To wire up our nervous system properly, neurons must elongate their axons during development to reach their targets. This is no simple task, however. The complex morphology of axons and dendrites puts neurons among the most intricate and beautiful cells in the body. Knowledge of how neurons extend axons and dendrites, elongate at a particular rate, and stop growing at the proper time is critical to understanding the development of our nervous system, yet the regulation of these processes is poorly understood. Considerable attention in recent years has focused on understanding how growth cones are guided and steered through complicated pathways (for review, see Schmidt and Hall 1998;Mueller 1999), and even how neurons initiate new processes (for review, see Da Silva and Dotti 2002), but what mechanisms are involved in elongation itself? Are environmental signals needed to drive axon growth and, if so, what are the intracellular molecular mechanisms by which they induce elongation? What controls the rate of axon growth? How do CNS neurons know whether to extend axons or dendrites? Is the signaling of axon versus dendrite growth attributable to different extracellular signals, different neuronal states, or both? All of these questions bear critically on our understanding of axon growth and here I review recent answers and approaches to the above questions, and highlight their relevance during development, injury, and disease.

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“…The cells were fixed for 20 minutes in a buffer containing 4% formaldehyde with 400 mM sucrose in PBS at pH 7.4, and permeabilized for five minutes in fixation buffer containing 0.2% Triton-100 (25). The cells were subsequently incubated with primary rat monoclonal anti-tubulin antibody YL1/2 (1:1000; originally a gift from J.V.…”

Section: Immunofluorescence and Microscopymentioning

confidence: 99%

Cellular disorders induced by high magnetic fields

Valiron

Peris

Rikken

et al. 2005

Magnetic Resonance Imaging

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Purpose: To evaluate whether static high magnetic fields (HMFs), in the range of 10 -17 T, affect the cytoskeleton and cell organization in different types of mammalian cells, including fibroblasts, epithelial cells, and differentiating neurons.Materials and Methods: Cells were exposed to HMF for 30 or 60 minutes and subsequently assessed for viability. Cytoskeleton arrays and focal adhesions were visualized using immunofluorescence microscopy.Results: Cell exposure to HMF over 10 T in the case of cycling cells, and over 15 T in the case of neurons, affected cell viability, apparently because of cell detachment from culture dishes. In the remaining adherent cells, the organization of actin assemblies was perturbed, and both cell adhesion and spreading were impaired. Moreover, in the case of neurons, exposure to HMF induced growth cone retraction and delayed cell differentiation. Conclusion:Cell exposure to HMF (over 10T and 15 T in the case of cycling cells and neurons, respectively) affects the cell cytoskeleton, with deleterious effects on cell viability, organization, and differentiation. Further studies are needed to determine whether such perturbations, as observed here in cultured cells, have consequences in whole animals.

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Actions of cytochalasins on the organization of actin filaments and microtubules in a neuronal growth cone.

Cited by 813 publications

References 47 publications

Evidence for the Involvement of Tiam1 in Axon Formation

Evidence for the Involvement of Tiam1 in Axon Formation

How does an axon grow?

Cellular disorders induced by high magnetic fields

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